The specific aim of the proposed project is to use electrophysiological methods to study the lumbar epaxial motor units of the rat which constitute the final common pathway of the estrogen-dependent somatosensory reflex, lordosis. The ultimate goal is to define the sites of synaptic interaction between hormone-related neural circuits and the cutaneous reflex which is the substrate of the motor behavior. In awake animals performing lordosis, we have used fine wire bipolar electrodes with in situ amplified electromyography and concomitant axial movement recordings registered by a small mercury length gauge attached to lumbosacral vertebrae, and have ascertained that lateral longissimus and transverso-spinalis are part of the muscle profile of the reflex. We will continue these chronic EMG experiments while applying conditioning shocks to the lateral vestibular nucleus and nucleus gigantocellularis since chronic spinal rats do not perform lordosis but the integrity of the anterolateral quadrant of the spinal cord through which these nuclei project is sufficient and necessary for reflex performance. We have demonstrated a polysynaptic response in lateral longissimus (LL) which is evoked from the cutaneous receptive field of the reflex. We now plan to quantify the fraction of the total segmental motoneuron pool to LL that is recruited by reflex afferents. To accomplish this, the integrated response of the segmental muscle nerve following pudendal nerve stimulation will be compared to the integrated response evoked by antidromic stimulation to the homonymous ventral root. The cutaneous reflex response in LL can be recorded at the same latency and with the same probability in ovariectomized rats with and without estrogen replacement, but the probability of late discharges increases with hormone. Using paired trains of stimuli to the pudendal nerve in order to study the time course of late facilitation and to determine whether it is a consequence of preceding recurrent inhibition, we can compare the results in animals with both hormone conditions and postulate the synaptic site of action for estrogen-related neural inputs. Repeating these experiments after spinal transection will eliminate the predominant estrogen effect derived from descending pathways and reveal any residual effect due to direct hormone action on spinal neurons. We will also test the hypothesis that an action of estrogen in the spinal cord is to modulate PAD.